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1.
Chinese Journal of Contemporary Pediatrics ; (12): 169-175, 2022.
Article in English | WPRIM | ID: wpr-928583

ABSTRACT

OBJECTIVES@#To systematically evaluate the effect of prophylactic use of hydrolyzed protein formula on gastrointestinal diseases and physical development in preterm infants.@*METHODS@#A computerized search was performed in the databases including China National Knowledge Infrastructure, Wanfang Data, Weipu, PubMed, Embase, and the Cochrane Library to identify randomized controlled trials of the effect of prophylactic use of hydrolyzed protein formula on gastrointestinal diseases and physical growth in preterm infants. RevMan 5.3 software was used to perform a Meta analysis for the included studies.@*RESULTS@#A total of 7 randomized controlled studies were included. The results of Meta analysis showed that compared with the whole protein formula, the prophylactic use of hydrolyzed protein formula could reduce the risk of neonatal necrotizing enterocolitis (RR=0.40, P=0.04) and feeding intolerance (RR=0.40, P=0.005), and had no significant effect on the growth of weight, length and head circumference (P>0.05).@*CONCLUSIONS@#Compared with the whole protein formula, the prophylactic use of hydrolyzed protein formula in preterm infants may reduce the occurrence of necrotizing enterocolitis and feeding intolerance, and can meet the nutrient requirement of physical development. However, the evidence is limited, and the results of this study cannot support the routine prophylactic use of hydrolyzed protein formula in preterm infants.


Subject(s)
Humans , Infant , Infant, Newborn , Enterocolitis, Necrotizing/prevention & control , Gastrointestinal Diseases/prevention & control , Infant Formula/chemistry , Infant, Low Birth Weight , Infant, Premature , Randomized Controlled Trials as Topic
2.
Acta Academiae Medicinae Sinicae ; (6): 208-212, 2022.
Article in Chinese | WPRIM | ID: wpr-927867

ABSTRACT

Objective To study the influence of recombinant bovine basic fibroblast growth factor as an adjuvant therapy on scar alleviation and inflammatory cytokines in patients with atrophic acne scar. Methods The random number table was employed to randomly assign 120 patients with atrophic acne scar into a test group and a control group.Both groups of patients were treated with CO2 lattice laser.After the operation,the control group was routinely smeared with erythromycin ointment and the test group was coated with recombinant bovine basic fibroblast growth factor gel.The clinical efficacy,clinical indicators,scar alleviation,and inflammatory cytokine levels before and after treatment were compared,and adverse reactions were counted. Results The test group had higher total effective rate(P=0.040) and lower total incidence of adverse reactions(P=0.028) than the control group.Compared with the control group,the test group showcased short erythema duration after treatment(P=0.025),early scab forming(P=0.002),and early edema regression(P<0.001).After treatment,the proportion of grade 1 scars graded by Goodman and Baron's acne scar grading system in the test group and control group increased(P=0.001,P=0.027),and the proportion of grade 4 scars decreased(P<0.001,P=0.034).Moreover,the proportion of grade 1 scars in the test group was higher than that in the control group(P=0.031) after treatment,and the proportion of grade 4 scars presented an opposite trend(P=0.031).After treatment,the levels of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in both groups declined(all P<0.001),and the test group had lower TNF-α and IL-1β levels than the control group(all P<0.001). Conclusion The recombinant bovine basic fibroblast growth factor gel as an adjuvant therapy of CO2 lattice laser can effectively alleviate the atrophic acne scar,relieve local inflammatory reaction,and has good curative effect and less adverse reactions.


Subject(s)
Animals , Cattle , Humans , Acne Vulgaris/drug therapy , Atrophy/complications , Carbon Dioxide , Cicatrix/pathology , Fibroblast Growth Factor 2/therapeutic use , Treatment Outcome , Tumor Necrosis Factor-alpha
3.
Journal of Experimental Hematology ; (6): 1559-1565, 2017.
Article in Chinese | WPRIM | ID: wpr-301688

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the regulation of Bruton's tyrosine kinase (Btk) and to explore its possible mechanism.</p><p><b>METHODS</b>After treatment with the proteasome inhibitors and/or phorbol esters (PMA), the mRNA and protein expression level of Btk was detected by RT-PCR and Western blot, respectively. The ubiquitination level of Btk in B lymphoblastoid A20 cells was estimated after stimulation via the crosslinking of BCR with anti-IgM antibody. The cotransfection of COS-7 cell with Btk, ubiquitin and Cbl was performed, then the ubiquitination level of Btk was measured. The Btk ubiquitination level was detected after ectopic expression of ubiquitin transfected with the wild type or triple mutant of Ub (K29R, K48R, K63R) . Mono-ubiquitination of Btk was detected with antibodies preferentially against monovalent ubiquitin; in addition, the protein expression levels of chloroquine-treated stably transfected cells expressing Btk-GFP were detected by Western blot, and quantified with the strength of GFP fluorescence.</p><p><b>RESULTS</b>In the presence of proteasome-specific inhibitors and/or PMA, steady-state levels of Btk protein were reduced due to decrease of transcription. Posttranslational modification of Btk by ubiquitination was observed, which was related with the level of Btk expression and activation. The E3 ubiquitin ligase Cbl, which binds to Btk, was also found to ubiquitinate this kinase. Altogether, the data of this study strongly suggest that Btk is regulated by poly- and/or mono-ubiquitination events.</p><p><b>CONCLUSION</b>The Btk protein is dictated by its expression level through the ubiquitination pathway.</p>

4.
Journal of Experimental Hematology ; (6): 754-760, 2017.
Article in Chinese | WPRIM | ID: wpr-271924

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effect of Ibrutinib on the chemoresistance mediated by SDF-1α/CXCR4 axis in ALL cells.</p><p><b>METHODS</b>Flow cytometry was used to detect the apoptosis of cell line and expression of surface membrane CXCR4, Western blot was used to determine the expression level of CXCR4, ERK and Bcl-xL proteins, qPCR was used to assay the mRNA level of CXCR4.</p><p><b>RESULTS</b>Ibrutinib enhanced the apoptosis induced by adriamycin(ADR) (17.100±4.3% to 28.133±3.16%); Ibrutinib inhibited the phosphorylation of CXCR4 induced by SDF-1α and with concentration- and time- dependent manner (r=-0.99659, r=-0.99764, r=-0.99980). Ibrutinib inhibited the expression and activity of CXCR4 downstream signaling molecules pERK and BCL-xL.</p><p><b>CONCLUSION</b>Ibrutinib can enhance the sensitivity of SUP-B15 to ADR, reverse SDF-1α/CXCR4-mediated chemoresistance in Phacute lymphoblastic leukemia cells. This mechanism of ibrutinib may be assosiated with inhibiting CXCR4/ERK/BCL-xL.</p>

5.
Chinese Medical Journal ; (24): 4054-4059, 2013.
Article in English | WPRIM | ID: wpr-236106

ABSTRACT

<p><b>BACKGROUND</b>Oxidative Stress and p38 mitogen-activated protein kinase (p38MAPK) play a vital role in renal fibrosis. Pioglitazone can protect kidney but the underlying mechanisms are less clear. The purpose of this study was to investigate the effect of pioglitazone on oxidative stress and whether the severity of oxidative stress was associated with the phosphorylation level of p38MAPK.</p><p><b>METHODS</b>Rat mesangial cells were cultured and randomly assigned to control group, high glucose group and pioglitazone group. After 48-hour exposure, the supernatants and cells were collected. The protein levels of p22(phox), p47(phox), phosphorylated p38MAPK, total p38MAPK were measured by Western blotting. The gene expressions of p22(phox), p47(phox) were detected by RT-PCR. The levels of intracellular reactive oxygen species (ROS) were determined by flow cytometry. The levels of superoxide dismutase (SOD) and maleic dialdehyde (MDA) in the supernatant were determined respectively.</p><p><b>RESULTS</b>Compared with the control group, the expression levels of p22(phox), p47(phox), phospho-p38 and ROS significantly increased, activity of SOD decreased in high glucose group, while the level of MDA greatly increased (P < 0.01). Pioglitazone significantly suppressed p22(phox), p47(phox) expressions and oxidative stress induced by high glucose. The expressions of p22(phox), p47(phox), phospho-p38MAPK and ROS generation were markedly reduced after pioglitazone treatment (P < 0.05). The activity of SOD in the the supernatant increased (P < 0.05), while the level of MDA decreased greatly by pioglitazone (P < 0.05). The level of oxidative stress was associated with the phosphorylation level of p38MAPK (P < 0.01).</p><p><b>CONCLUSION</b>Pioglitazone can inhibit oxidative stress through suppressing NADPH oxidase expression and p38MAPK phosphorylation.</p>


Subject(s)
Animals , Rats , Blotting, Western , Glucose , Pharmacology , Mesangial Cells , NADPH Oxidases , Genetics , Metabolism , Reactive Oxygen Species , Metabolism , Thiazolidinediones , Pharmacology , p38 Mitogen-Activated Protein Kinases , Genetics , Metabolism
6.
International Journal of Oral Science ; (4): 129-134, 2012.
Article in English | WPRIM | ID: wpr-358214

ABSTRACT

Enamel crystals are unique in shape, orientation and organization. They are hundreds of thousands times longer than they are wide, run parallel to each other, are oriented with respect to the ameloblast membrane at the mineralization front and are organized into rod or interrod enamel. The classical theory of amelogenesis postulates that extracellular matrix proteins shape crystallites by specifically inhibiting ion deposition on the crystal sides, orient them by binding multiple crystallites and establish higher levels of crystal organization. Elements of the classical theory are supported in principle by in vitro studies; however, the classical theory does not explain how enamel forms in vivo. In this review, we describe how amelogenesis is highly integrated with ameloblast cell activities and how the shape, orientation and organization of enamel mineral ribbons are established by a mineralization front apparatus along the secretory surface of the ameloblast cell membrane.


Subject(s)
Humans , Ameloblasts , Chemistry , Cell Biology , Amelogenesis , Physiology , Basement Membrane , Chemistry , Crystallization , Dental Enamel , Chemistry , Dental Enamel Proteins , Bodily Secretions , Tooth Calcification
7.
Journal of Southern Medical University ; (12): 1059-1062, 2011.
Article in Chinese | WPRIM | ID: wpr-235197

ABSTRACT

<p><b>OBJECTIVE</b>To explore the association between renal transforming growth factor-β1 (TGF-β1) and the expressions of α3 and β1 integrins and observe the effect of irbesartan on their expressions in diabetic rats.</p><p><b>METHODS</b>Thirty 8-week-old male Wistar rats were randomly divided into normal control group (n=7), diabetic control group (n=14) and irbesartan group (n=9). Rat models of diabetes were established by a single peritoneal injection of streptozotocin (STZ), and 4 weeks later the rats received irbesartan treatment for 8 weeks. Enzyme-linked immunosorbent assay (ELISA) was used to measure the urinary albumin excretion rate, and PAS staining was utilized to observe the renal pathologies. Immunohistochemistry was performed for semi-quantitative determination of podocyte density, and real-time RT-PCR was used to detect the renal TGF-β1 and α3/β1 integrin mRNA expressions.</p><p><b>RESULTS</b>In diabetic rats, the expression of renal TGF-β1 mRNA was significantly increased, while α3 and β1 integrin mRNA expressions and podocyte density significantly decreased with increased proteinuria. Irbesartan obviously improved such changes.</p><p><b>CONCLUSION</b>In diabetic rats renal TGF-β1 can regulate α3 and β1 integrin mRNA expressions to reduce the number of podocytes, and inhibition of this pathway may be one of the mechanisms of the renal protective effect of irbesartan.</p>


Subject(s)
Animals , Male , Rats , Biphenyl Compounds , Pharmacology , Diabetes Mellitus , Metabolism , Diabetic Nephropathies , Metabolism , Integrin alpha3 , Metabolism , Integrin beta1 , Metabolism , Kidney , Metabolism , Rats, Wistar , Tetrazoles , Pharmacology , Transforming Growth Factor beta1 , Metabolism
8.
Journal of Southern Medical University ; (12): 1336-1338, 2010.
Article in Chinese | WPRIM | ID: wpr-336185

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effect of irbesartan on angiotensin-converting enzyme 2 (ACE2) mRNA expression in diabetic rat myocardium.</p><p><b>METHODS</b>Thirty 8-week-old male Wistar rats were randomly divided into control group (n=7), diabetic model group (n=14) and irbesartan group (n=9). Diabetes was induced by a single intraperitoneal injection of STZ (55 mg/kg), a blood glucose>16.7 mmol/L 72 h after the injection indicated successful establishment of diabetes. Four weeks after the modeling, the rats in irbesartan group were given 50 mg/kg irbesartan. ELISA was used to measure myocardial AngII content in the rats, and myocardial ACE2 mRNA expression was determined by real-time PCR.</p><p><b>RESULTS</b>Myocardial AngII level in the diabetic model group was significantly higher than that in the control group (P<0.001). Irbesartan administration significantly lowered cardiac AngII levels in the diabetic rats (P<0.001). The rats in irbesartan group showed significantly increased myocardial ACE2 mRNA expression compared with those in the control and diabetic rat groups (P<0.05).</p><p><b>CONCLUSION</b>Irbesartan can increase ACE2 mRNA expression in the myocardium, which might be one of the mechanisms underlying its effect in improving the cardiac function in diabetic rats.</p>


Subject(s)
Animals , Male , Rats , Biphenyl Compounds , Pharmacology , Diabetes Mellitus, Experimental , Myocardium , Peptidyl-Dipeptidase A , Genetics , Metabolism , RNA, Messenger , Genetics , Metabolism , Random Allocation , Rats, Wistar , Tetrazoles , Pharmacology
9.
Chinese Journal of Epidemiology ; (12): 720-725, 2009.
Article in Chinese | WPRIM | ID: wpr-261344

ABSTRACT

Objective To analyze the genetic characteristics of HIV-1 CRF01_AE strains prevailing in. the four provinces of southern China. Methods Plasma samples were collected from the newly diagnosed HIV-1 individuals reported in 2006 in Guangdong, Guangxi, Jiangxi and Hunan province. The gag and env gene fragments were amplified from RNA template extracted from plasma using RT and nested PCR methods. CRF01_AE sequences were analyzed by phylogcnetie methods and characterized by calculating the genetic distance and Entropy analysis. Results Two main epidemic clusters were found to exist in the CRF01 AE strains from 210 HIV-1 CRF01 AE infected individuals collected in the 4 provinces, southern China. It was found that no international reference strain was closely correlated with cluster Ⅰ , which including 123 samples. The strains in cluster Ⅱ, consisting 57 cases of samples, were closely related with the strains identified in Vietnam. Genetic distance analysis of gag and env genes showed that the diversity of cluster Ⅰ was obviously less than that of cluster Ⅱ. Data on nucleotide polymorphism showed that nucleotides compositions of 42 sites in gag and 40 sites in env wer esignificantly different between the two clusters. When compared with cluster Ⅱ , the polymorphism decreased at 61 nucleotide sites but increased at 21 sites in cluster Ⅰ. Conclusion This was the first report describing that two main epidemic clusters were existed in CRF01_AE strains prevailing in the 4 provinces, Southern China. The vires in cluster Ⅰ was the dominant strain in this region, with shorter period of circulation and higher proportion seen in the HIV-infected population, which might belong to CRF01_AE strain with certain features facilitating the spread of the virus. The virus in cluster Ⅱ was highly homology with the CRF01_AE strains from Vietnam, and seemed to have had several events of epidemics in populations in border regions of China and Vietnam.

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